Dramatic neuronal rescue with prolonged selective head cooling after ischemia in fetal lambs.

@article{Gunn1997DramaticNR,
  title={Dramatic neuronal rescue with prolonged selective head cooling after ischemia in fetal lambs.},
  author={Alistair J. Gunn and Tania R. Gunn and Harmen H. de Haan and Chris Edward Williams and Peter D. Gluckman},
  journal={The Journal of clinical investigation},
  year={1997},
  volume={99 2},
  pages={
          248-56
        },
  url={https://api.semanticscholar.org/CorpusID:42458500}
}
Selective head cooling, maintained throughout the secondary phase of injury, is noninvasive and safe and shows potential for improving neonatal outcome after perinatal asphyxia.
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Neuroprotection With Prolonged Head Cooling Started Before Postischemic Seizures in Fetal Sheep

Delayed selective head cooling begun before the onset of postischemic seizures and continued for 3 days may have potential to significantly improve the outcome of moderate to severe hypoxic-ischemi encephalopathy.

Cerebral Hypothermia Is Not Neuroprotective When Started after Postischemic Seizures in Fetal Sheep

Delayed prolonged head cooling begun after the onset of postischemic seizures was not neuroprotective, highlighting the importance of intervention in the latent phase, after reperfusion but before the start of secondary injury.

How Long is Too Long for Cerebral Cooling after Ischemia in Fetal Sheep?

Extending the duration of delayed therapeutic hypothermia from 3 to 5 days did not improve outcomes after severe ischemia, and was associated with reduced neuronal survival in some regions.

Differential effects of hypothermia on early and late epileptiform events after severe hypoxia in preterm fetal sheep.

Neuroprotection with delayed, prolonged head cooling after a severe asphyxial insult in the preterm fetus was associated with potent, specific suppression of epileptiform transients in the early recovery phase but not of numbers of delayed seizures.

The effect of cerebral hypothermia on white and grey matter injury induced by severe hypoxia in preterm fetal sheep

Delayed, prolonged head cooling after a profound hypoxic insult in the preterm fetus was associated with a significant reduction in loss of neurons and immature oligodendroglia, with evidence of EEG and haemodynamic improvement after 3 days recovery, but also with a persisting reduction in proliferation of cells in the periventricular region.

How long is sufficient for optimal neuroprotection with cerebral cooling after ischemia in fetal sheep?

Findings show that head cooling for 48’h is partially neuroprotective, but is inferior to cooling for 72 h after cerebral ischemia in fetal sheep, which strongly suggests that deleterious inflammation can be reactivated by premature rewarming.

Epileptiform Activity During Rewarming from Moderate Cerebral Hypothermia in the Near-Term Fetal Sheep

Rapid rewarming after a prolonged interval of therapeutic hypothermia can be associated with a transient increase in epileptiform events but does not seem to have significant adverse implications for neural outcome.

Extending the duration of hypothermia does not further improve white matter protection after ischemia in term-equivalent fetal sheep

Delayed cerebral hypothermia partially protected white matter after global cerebral ischemia in fetal sheep, and may be associated with greater numbers of residual microglia.

Effective Selective Head Cooling during Posthypoxic Hypothermia in Newborn Piglets

It is reported for the first time a study, which by direct measurement of deep intracerebral temperatures, validates the cooling cap as an effective method of selective brain cooling in a newborn animal hypoxia-ischemia model.

Induced cerebral hypothermia reduces post-hypoxic loss of phenotypic striatal neurons in preterm fetal sheep

...

35 References

Mild Hypothermia after Severe Transient Hypoxia-Ischemia Ameliorates Delayed Cerebral Energy Failure in the Newborn Piglet

It is concluded that mild hypothermia after a severe acute cerebral hypoxicischemic insult ameliorated delayed energy failure in newborn piglets.

Posthypoxic cooling of neonatal rats provides protection against brain injury.

Posthypoxic hypothermia reduces brain damage in awake, unrestrained 7 day old rats, and is associated with reduced brain temperature and blood chemistry studies.

Delayed and prolonged post-ischemic hypothermia is neuroprotective in the gerbil

Postischemic moderate hypothermia inhibits CA1 hippocampal ischemic neuronal injury

Delay in cooling negates the beneficial effect of mild resuscitative cerebral hypothermia after cardiac arrest in dogs: A prospective, randomized study

Mild, resuscitative cerebral hypothermia induced immediately with reperfusions after cardiac arrest improves cerebral functional and morphologic outcome, whereas a delay of 15 mins in initiation of cooling after reperfusion may not improve functional outcome, although it may slightly decrease tissue damage.

Mild hypothermic intervention after graded ischemic stress in rats.

It is indicated that mild postischemic whole-body hypothermia ameliorates neuronal survival when ischemia lasts 8 minutes but not 12 minutes, and no differences were detected in any area of the hippocampus between the 12-minute normothermic and the 12 -minute hypothermic groups.

The Effect of Prolonged Modification of Cerebral Temperature on Outcome after Hypoxic-Ischemic Brain Injury in the Infant Rat

Hypothermia spanning both the first 6 h and from 6 to 72 h after injury was needed to improve outcome, and exposure to the thermoneutral environment exacerbated the injury.

Time course of intracellular edema and epileptiform activity following prenatal cerebral ischemia in sheep.

The secondary decrease of extracellular space indicates that a progressive loss of membrane function started with the onset of postischemic epileptiform activity, and the increased metabolic load of the epilepsy activity may have worsened this delayed deterioration.

Effects of hypothermic metabolic suppression on hippocampal glutamate concentrations after transient global cerebral ischemia.

It is concluded that hypothermic inhibition of glutamate release during episodes of transient ischemia may significantly contribute to neuronal protection.

Suppression of postischemic epileptiform activity with MK‐801 improves neural outcome in fetal sheep

It is suggested that N‐methyl‐D‐aspartate‐mediated epileptiform activity that develops after a global hypoxic‐ischemic insult worsens neuronal outcome in the immature brain.